Now that a broad base in the metabolism of copper by the normal rat and its liver has been established, alterations in the kinetics will be evaluated in copper-deficient and copper-laden rats, pregnant rats and cyclohexamide treated rats or their livers. Techniques will include use of intact rats, biliary fistula rats, isolated perfused rat livers and subcelluar heptic particles. Certain aspects of Wilson's disease have already been simulated by copper-deficient and copper laden rats; these studies will be extended. The function of ceruloplasmin will be explored further by infusion of labeled ceruloplasmin into normal and abnormal rats. Certain organs seem to accept copper only from ceruloplasmin while others may apparently take up "free" copper.